Open antireflux surgery has evolved to be a safe, reliable, and highly effective operation. Under usual circumstances, about 10% of patients will have significant post-fundoplication symptoms, but significant dysphagia is unusual. Some minimal dysphagia occurs in most patients immediately after operation [1] and mild dysphagia occurs in up to 20% of patients having open antireflux surgery but is usually transient and resolves spontaneously or with dilations. Significant dysphagia has been reported in up to 28% of patients with various antireflux procedures related to the underlying pathology, surgical error, intrinsic failures of the procedure or to incorrect diagnosis. Although dysphagia following laparoscopic fundoplication has been common, significant dysphagia following open antireflux surgery is almost always associated with severe strictures or with complications and errors in surgery. It may be due to a variety of causes and usually cannot be solved by a simple reconstruction of the fundoplication and medications [2].

Incorrect diagnosis

Anti-reflux surgery will change neither esophageal motility nor transit time. Patients who have underlying esophageal dysmotility not related to reflux disease will not be helped by antireflux surgery. Esophageal motility studies are essential in the diagnosis of patients with reflux disease to exclude those with defined or undefined motility disorders with inadaquate peristalsis. Especially with circumferential fundoplication, even a properly performed oparation can cause significant dysphagia by partially obstructing the esophagus.

The common incorrect diagnoses for which antireflux surgery has been done are:

- malignancy at the esophagogastric junction or in the stomach causing pseudo-achalasia with obstruction.

Pathology

The pathology of the esophageal disease itself either related to reflux or to underlying esophageal abnormalities can cause dysphagia. Strictures, especially those requiring multiple dilations and those associated with Barrett's esophagus without malignancy will frequently lead to postoperative dysphagia because of residual inflammation or constriction of the esophagus. A small number (approximately 3%), of patients with severe strictures will not be amenable to dilation and fundoplication. These patients will subsequently require resection or interposition.

The patients with connective tissue disorders, especially those with scleroderma, are a separate category. These patients have severe esophagitis with fibrosis and inadequate peristalsis. They frequently have dysphagia as a presenting symptom which can persist despite a partial fundoplication because of aperistalsis.

A special group of patients who have persistent dysphagia despite properly performed and successful antireflux surgery are those with familial dysautonomia. In these patients, incoordination of swallowing and esophageal peristalsis causes persistent dysphagia. Feeding and decompressive gastrostomy is therefore a necessary part of the antireflux surgery in these patients [3].

An additional group in which the esophageal function has been effectively damaged and/or destroyed are those patients with re-operative antireflux surgery after failed antireflux operations. Results are never as satisfactory in this group of patients with primary operation and are less satisfactory with each successive operation. Dysphagia in these patients can only be corrected by resection [4].

Technical problems

The most common cause for significant dysphagia after open antireflux surgery is technical error in the performance of the operation. The common problems are crural closure, malposition of the fundoplication and the use of prostheses.

Crural closure

Crural closure is a necessary part of all antireflux operations. Crural closure is necessary to improve the pinchcock mechanism and to maintain the gastroesophageal junction and the fundoplication in the abdomen. Failure to close the crura or too loose a closure of the crura can result in a paraesophageal hernia with migration of the fundus and the fundoplication into the posterior mediastinum. Angulation of this entire mechanism is a cause of dysphagia.

A more common problem is too tight a crural closure. Crural closure should be done posteriorly using heavy sutures but the approximation of the crura around the esophagus must be loose enough to permit normal esophageal function. The use of reinforcing materials, such as polypropylene mesh can cause a dense inflammatory reaction with late scarring and tightening of the crural closure and should be avoided. A crural closure of appropriate size can best be assured by placement of an adequate size bougie when the sutures are tied during crural closure. If overly tight crural closure is the cause of dysphagia dilation with bougie or balloon is usually unsuccessful. Re-operation and reconstruction is necessary to release the external compression which narrows the esophagus.

Malposition of the fundoplication

To be effective, the fundoplication must be short enough, loose enough and properly placed. Too long a fundoplication is a frequent cause of dysphagia and current data suggests that the fundoplication should be limited to three centimeters. Too tight a fundoplication can be avoided by adequate mobilization of the fundus and division of the posterior gastric adhesions. Division of a number of short gastric vessels is also necessary in most patients. Avoidance of prosthetic materials which produce inflammatory reaction and suture of the fundoplication over an adequate bougie are essential. The fundoplication must be fashioned around the esophagus with its lower edge at the esophagogastric junction if the Belsey, Toupet, Dor, or Nissen type of wrap is used. The repair must be adequately secured to the stomach, esophagus and/or crura to assure its position. Slippage of a loose Nissen wrap either onto the stomach causing an hourglass deformity or herniation of the stomach inside the Nissen will cause dysphagia.

Prostheses

The use of prostheses, especially of the Angelchick variety, is associated with a very high incidence of dysphagia. Severe dysphagia in up to 28% of patients has been observed. The severity of dysphagia has been exaggerated when the Angelchick prosthesis migrates. It is also accentuated in any patients who have pre-operative dysphagia. Concern about the effects of prosthetic materials early and late makes any significant amount of prosthetic reinforcement a high risk for dysphagia. The Collis gastroplasty is also associated with a 17% incidence of dysphagia if the operation is not done accurately [5].

Conclusion

Successful antireflux surgery without dysphagia requires correct diagnosis and appropriate surgical technique. Those mild dysphagias due to edema will resolve spontaneously or respond to simple bouginage. Those due to technical error or inappropriate operation can only be corrected by appropriate remedial surgery. Results of these operations are never as successful as the primary operation.